Disorders of blood plasma lipid metabolism. Symptoms of metabolic disorders. Lipid metabolism: what indicates disturbances

Metabolism in the body largely depends on individual factors, including hereditary ones. Wrong image life and lack of mobility lead to the fact that the body can no longer cope with its tasks, and metabolic processes slow down. As a result, waste products do not leave the body as efficiently; many wastes and toxins remain in the tissues for a long time, and even tend to accumulate. What are the causes of the disorder, and how to get rid of them?

Can disruption of processes in the body cause excess weight gain?

The essence metabolic processes organism - a number of specific chemical reactions, due to which the functioning of all organs and biological systems. Metabolism consists of two processes that are opposite in meaning - anabolism and catabolism. In the first case, complex compounds are formed from simpler ones, in the second, complex organic matter is broken down into simpler components. Naturally, the synthesis of new complex compounds requires large energy expenditures, which are replenished through catabolism.

Regulation of metabolic processes occurs under the influence of enzymes, hormones and other active ingredients. In the natural course of metabolic processes, disturbances may occur, including those leading to excessive weight gain. Restore normal metabolism without use medicines almost impossible. Before losing weight, you should definitely consult with an endocrinologist.

In most cases overweight not explained endocrine disorders– they account for only about 10 percent of cases. Situations are common when there are no disturbances with hormones, when tests do not show any deviations from normal values, but at the same time it is not possible to get rid of excess weight. The reason is a slowdown in metabolism and poor nutrition.

Reasons for slowing down metabolic processes in the body

One of the common factors is a person’s desire to lose excess weight as quickly as possible, without regard to the consequences. For example, these could be diets that involve a sudden change in diet and a transition to low-calorie foods. For the body, such diets are a huge stress, and therefore very often it cannot be avoided without certain disorders.

Even if the diet is successful and the desired body weight is achieved, further weight loss will be much more difficult, and the problem will always get worse. Previously effective diets cease to give the desired result, maintaining shape becomes more difficult, or even impossible in principle. All this indicates a slowdown in metabolic processes, and it is necessary to normalize them, return them to their original values.

Restoration processes will take a lot of time and effort, but such activities will certainly yield positive results. If you plan to reduce body weight, with a normal metabolism it will be easier to do this, and with a long-term effect without any extraordinary effort. In order not to harm the body, you should eat quite often, but little by little.

Lipid metabolism: what indicates disturbances?

Normal lipid metabolism prevents damage, helps replenish the body's energy reserves, provides heating and thermal insulation internal organs. An additional function in women is to help the body produce a number of hormones (mainly related to ensuring the functioning of the reproductive system).

With a number of disorders, it may turn out that there is an excess amount of lipids in the body. This is indicated by atherosclerotic processes, increased cholesterol in the blood, and a sharp increase in excess weight. Disturbances can be caused by pathologies of the endocrine system, improper diet and diet, and diabetes. To accurately understand the problem, you should consult a doctor and undergo appropriate examinations.

There is also a reverse process when there are too few lipids. In women this may result in problems menstrual cycle, in women and men – in severe loss hair and various inflammations skin. As a result, the person becomes exhausted and kidney problems may begin. The problem most often occurs with poor diet or prolonged fasting. Diseases of the digestive and cardiovascular systems may also be the cause.

To quickly lose weight, many people resort to special diets, capable of making metabolism faster for a while. This is reflected in the body not only by weight loss, but also by many harmful effects. Fats are a reserve of energy “for later,” and stress in nutrition only increases the body’s desire to save and put aside any extra calories. Even if the diet gives short-term positive effect, even a short-term refusal to diet will bring back the kilograms, and it will be even more difficult to lose them again.

Natural metabolism can also be restored with the help of medications. The most common medications are described below.

Medicines to improve metabolism

Many medications have been developed that can help normalize metabolic processes in the body. Self-administration of these medications is not allowed; prior consultation with a doctor (nutritionist) is always necessary. It is worth paying attention to the following medications:

• Oxandrolone and Methylandrostenediol are steroids, thanks to which muscles grow faster and less fat is deposited. Use with extreme caution!
• Reduxin - can be taken after a small meal to get a full feeling of fullness and thereby avoid stress.
• Orsoten and Xenical are medications that prevent the absorption of fats.
• Glucophage is a means to accelerate and enhance lipid metabolism.
• Formavit, Metaboline - means of regulating the metabolism of carbohydrates and fats.

There are many other ways to normalize metabolism, including eating certain foods. Key product recommendations are listed below.

Nuts, fish, chicken, milk, cottage cheese (low-fat or low-fat), as well as vegetables, berries and fruits can have a positive effect. Even tea and coffee can be beneficial, as they are stimulants. Some spices also have positive influence, but they should be consumed in moderation. The following discusses the main useful material in the products:

Do not neglect iodine. Metabolism largely depends on work thyroid gland, but for many people this organ is problematic, even leading to surgery to remove it. Seafood is good for improving the functioning of the thyroid gland.

Folk remedies to speed up metabolism

If there is any suspicion of malfunction metabolism, you should consult a doctor to determine accurate diagnosis and treatment prescriptions. As a rule, treatment is medicinal, but it must be combined with various physical procedures. You can also turn to the experience of traditional medicine, many natural remedies may be a good addition to medications. These may include the following fees:

• A mixture of chamomile, hawthorn, St. John's wort and knotweed (water infusion).
• Separately - fireweed, horsetail, strawberry leaves and stems, plantain leaves, viburnum.
• Various combinations medicinal herbs with dandelion.

Cannot be considered traditional medicine as a complete replacement for traditional medicine. All of these methods can be considered only as auxiliary, or as preventive.

Diet to improve metabolism

Special metabolic diets have been developed great amount, most come down to increasing the body's calorie expenditure by eating certain foods. It turns out that you can give up unnecessary restrictions on food, but still lose weight. The range of products usually offered is as follows: fatty fish, hot peppers, seaweed, coffee, leafy vegetables, tomatoes, grain bread, fruits - mainly citrus fruits, animal proteins, green tea.

All of these products are used in various quantities and combinations throughout the week. The exact menu can be found by opening the description of a specific diet.

Specials accepted vitamin complexes in small dosages. Vitamins are biologically active compounds; they participate in many processes occurring in the body and ensure normal metabolism. The most common means:

• B6 and B12 - good addition to metabolic diets.
• B4 - very important in low-calorie diets, helps cleanse cholesterol.
• B8 – maintains cholesterol levels, accelerates metabolic processes (especially in combination with B4).
• C – prevents excess accumulation of glucose, promotes general normalization body work.
• A – improves the absorption of iodine, has a positive effect on the thyroid gland.
• D – necessary for intensive growth of muscle tissue.

Also, products such as folic acid and Omega-3.

Biostimulants to enhance metabolism

Despite the “serious” name, biostimulants are the most common substances, many of which are found in the daily diet. These include linoleic acid(CLA), zinc, cahetin, selenium, capsaicin, caffeine. All of them are contained in products that can be bought in any store. You just need to choose options that contain biostimulants maximum amount. In the case of caffeine, you should stop drinking coffee as a drink while taking caffeine supplements.

You will find useful tips on speeding up your metabolism in the following video:

Restore metabolism and restore health

IN long term metabolic disorders can lead to excess weight gain and many health problems. There are many ways to not only restore, but also speed up metabolism, but doctors do not recommend the second option - you should not do something that was not originally intended by nature. As for restoring metabolism to an optimal level, this can and should be done - this is the best way improve health and cleanse the body.

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Lipid metabolism, in contrast to protein and carbohydrate metabolism, is diverse: fats are synthesized not only from fatty compounds, but also from proteins and sugars. They also enter food, breaking down into upper section gastrointestinal tract and being absorbed into the blood. Lipid levels are constantly changing and depend on many reasons. The metabolism of fats in the human body can easily be disrupted, and only a specialist knows how to restore or treat the disturbed balance.

Let's figure out how lipid metabolism occurs in the body, what happens during lipid imbalance and how to recognize its signs?

Textbooks for students medical universities lipid metabolism is a set of processes for the transformation of fats in the cells of the body and in the extracellular environment. In essence, these are all changes in fat-containing compounds when interacting with others, as a result of which lipid functions in the human body:

• providing energy (the breakdown of fats occurs with the separation of hydrogen atoms that combine with oxygen atoms, which leads to the formation of water with the release large quantity heat);
• the reserve of this energy (in the form of lipid deposition in fat depots - subcutaneous and visceral tissue, cell mitochondria);
• stabilization and regeneration of cytoplasmic membranes (fats are part of all cell membranes);
• participation in synthesis biologically active substances (steroid hormones, prostaglandins, vitamins A and D), as well as signaling molecules that transmit information from cell to cell;
• thermal insulation and shock absorption of internal organs;
• fall prevention lung tissue(some lipids are integral part surfactant);
• participation in the cellular response to oxidative stress caused by free radicals, and preventing the development of associated pathologies;
• protection of red blood cells from hemotropic poisons;
• recognition of antigens (protruding processes of lipid complexes of cytoplasmic membranes act as receptors, the main of which is agglutination in case of blood incompatibility according to the AB0 system);
• participation in the process of digesting dietary fats;
• the formation of a protective film on the surface of the skin, protecting it from drying out;
• synthesis of the main hormone that regulates its own (fat) metabolism (this substance is leptin).

Since we are talking about hormonal regulation, it is worth mentioning other biologically active compounds that affect lipid balance: insulin, thyrotropin, somatotropin, cortisol, testosterone. They are synthesized by the pancreas and thyroid glands, pituitary gland, adrenal cortex, male testes and female ovaries. Insulin promotes the formation of fat; other hormones, on the contrary, accelerate its metabolism.

Fats contained in all living cells, divided into several groups:

• fatty acids, aldehydes, alcohols;
• mono-, di- and triglycerides;
• glyco-, phospholipids and phosphoglycolipids;
• waxes;
• sphingolipids;
• sterol esters (including cholesterol, chemical composition which is an alcohol, but plays a huge role in lipid metabolism disorders).

There are several more highly specific fats, and all of them are participants in metabolic processes. In the neutral state, lipids are found only inside cells; their circulation in the bloodstream is impossible due to high probability development of fatty blockage small vessels. That's why nature provided them connection with transport proteins. Such complex connections called lipoproteins. Their anabolism occurs mainly in the liver and in the epithelium of the small intestine.

To determine the state of lipid metabolism, a blood test is performed for a lipid profile. It is called a lipid profile, and includes indicators of different fractions of lipoproteins (high, low and very low density), all cholesterol and triglycerides contained in them. The norms for lipid metabolism indicators vary depending on gender and age, and are summarized in a single table (for women and men), which is popular among doctors.

What processes does lipid metabolism involve?

Lipid metabolism goes through a certain sequence of stages:

1. digestion of fats entering the digestive tract;
2. connection with transport proteins and absorption into blood plasma;
3. synthesis of own lipids and similar binding to proteins;
4. transport of fat-protein complexes to organs through blood and lymphatic lines;
5. metabolism in the blood and inside cells;
6. transport of breakdown products to excretory organs;
7. removal of end products of metabolism.

The biochemistry of all these processes is very complex, but the main thing is to understand the essence of what is happening. To describe them briefly, lipid metabolism looks like this: having connected with carriers, lipoproteins travel to their destination, are fixed on cell receptors specific to them, and release essential fats, thereby increasing its density.

Next, most of the “impoverished” compounds return to the liver, are converted into bile acids and excreted into the intestines. To a lesser extent, the products of lipid metabolism are pushed directly from the cells of the kidneys and lungs into the external environment.

Considering the presented diagram fat metabolism, the dominant role of the liver in it becomes clear.

The role of the liver in fat metabolism

In addition to the fact that the liver itself synthesizes the main components of lipid metabolism, it is the liver that first receives the fats absorbed in the intestines. This is explained by the structure circulatory system. It was not in vain that nature came up with a system portal vein- a kind of “customs control”: everything received from outside goes through a “dress code” under the supervision of liver cells. They inactivate harmful substances independently or initiate the process of their destruction by other cells. And everything useful is put into the inferior vena cava, i.e. into the general bloodstream.

Fats bind to proteins for transport. At first, fat-protein complexes contain very little protein, which provides density to the compounds. These are very low density lipoproteins. Then a little more protein is added, and their density increases (intermediate density lipoproteins). With the next binding of protein molecules, low-density lipoproteins are formed. These are precisely the compounds that are the main carriers of fats to the cells of the body.

The listed substances all enter the blood, but LDL makes up the bulk of them. This means that the concentration of low-density lipoproteins is the highest compared to other fat-protein complexes. There is a high concentration in the blood of high-density lipoproteins – spent and “impoverished”. Once again in the liver, they split off lipids, which bind to primary bile acids and amino acids. The formed lipid compounds are already an integral part of bile.

Bile is reserved in gallbladder, and when a bolus of food enters the intestine, it is released through the bile ducts into the lumen alimentary canal. There, lipids help break down food into absorbable components. Unused fats during food processing return to the bloodstream and are sent to the liver. And everything starts anew.

The processes of synthesis, breakdown and excretion occur constantly, and the indicators of lipid metabolism fluctuate all the time. And they depend on the season, time of day, duration of food intake and quantity physical activity. And it’s good if these changes do not go beyond the norm. What happens if lipid metabolism is disrupted and its markers are outside the normal range? In what situations does this happen?

Lipid metabolism disorders: causes and consequences

Failure of fat metabolism can occur when:

• absorption disorders;
• inadequate excretion;
• disruption of transportation processes;
• excessive accumulation of lipids in structures other than adipose tissue;
• disruption of intermediate lipid metabolism;
• excessive or insufficient deposition in the fatty tissue itself.

The pathophysiology of these disorders is different, but they lead to the same result: dyslipidemia.

Malabsorption and increased excretion

Deterioration in lipid absorption develops when there is a small amount of the lipase enzyme, which normally breaks down fats into absorbable components, or its insufficient activation. Such conditions are signs of pancreatitis, pancreatic necrosis, sclerosis of the pancreas, pathology of the liver, gall bladder and excretory biliary tract, damage to the epithelial lining of the intestine, taking certain antibacterial drugs.

Fats are poorly absorbed and, as a result of interaction with calcium and magnesium, are still in the lumen of the gastrointestinal tract, resulting in the formation of insoluble and non-absorbable compounds. Consequently, foods rich in these minerals impair the absorption of lipids. Unabsorbed fats are excreted in excess feces which become greasy. The symptom is called steatorrhea.

Transportation disruption

Transport of fatty compounds is impossible without carrier proteins. Therefore, diseases, mainly hereditary, associated with impaired education or their complete absence, are accompanied by a disorder of lipid metabolism. These diseases include abetalipoproteinemia, hypobetalipoproteinemia and analphaproteinemia. Pathological processes in the liver, the main protein-synthesizing organ, also play an important role.

Accumulation of fat in and between highly specialized cells

The formation of fat droplets inside parenchymal cells develops due to increased lipogenesis, delayed oxidation, increased lipolysis, delayed excretion, lack of transport proteins. These factors lead to disruption of the removal of fat from cells and contribute to their accumulation. Fat droplets gradually grow in size and, as a result, completely push all organelles to the periphery. Cells lose their specificity, cease to perform their functions, and appearance no different from fatty ones. With advanced dystrophy, symptoms of failure of the affected organs occur.

The accumulation of fat deposits also occurs between cells - in the stroma. In this case, a violation of lipid metabolism leads to gradual compression of the parenchyma, and, again, to an increase in the functional failure of specialized tissues.

Intermediate metabolism disorder

Intermediate compounds in lipid metabolism are ketone bodies. They compete with glucose in energy production processes. And if there is little sugar in the blood, then to ensure the vital functions of the body, the production of ketone bodies increases. Their elevated levels in the blood are called ketoacidosis. It can be physiological (after heavy physical or psycho-emotional stress, later pregnancy) and pathological (related to diseases).

1. Physiological ketoacidosis does not reach high numbers and is short-term in nature, since ketone bodies quickly “burn out”, giving off necessary for the body energy.
2. Pathological ketoacidosis develops when the liver does not consume fatty acids only for the formation of triglycerides, but also uses them for the synthesis of ketone bodies (during fasting, diabetes mellitus). Ketones have a pronounced toxic effect, and with high ketoacidosis they are life-threatening.

Disorders of lipid metabolism in adipose tissue itself

Both lipogenesis and lipolysis occur in adipocytes. Normally they are balanced, thanks to hormonal and nervous regulation. Pathological changes depend on which of the processes predominates: with increased lipogenesis and reduced lipoprotein lipase activity, obesity develops (grade 1 obesity), and then a more pronounced increase in body weight, and with accelerated lipolysis, weight loss with the transition to cachexia (if timely intervention is not carried out) correction).

In addition, not only the volume of fat cells can change, but also their number (under the influence of genetic factors or morphogenesis factors - during early childhood, puberty, pregnancy, premenopausal period). But no matter at what stage of lipid metabolism the disorder occurs, dyslipidemia can manifest itself either as a decrease in fat levels or as an increase.

1. Hypolilipidemia, unless it is hereditary, is not clinically recognized for a long time. And only a blood test to determine the concentration of lipid profile indicators will help to understand what is happening: they will be reduced.
2. Hyperlipidemia, which is permanent, leads to weight gain, hypertension, cholelithiasis, atherosclerosis of the aorta and its branches, heart vessels (CHD) and brain. In this case, almost all indicators of lipid metabolism (except HDL) will be increased in the blood.

How to restore lipid metabolism in the body

To begin to restore something, need to know what is broken. Therefore, first they carry out diagnosis, and then correction. Diagnosis involves taking a blood test for a lipid profile. The rest of the examination depends on it: if the ratio of lipoproteins and triglycerides in the blood is disturbed, the immediate cause must be eliminated.

1. In case of gastrointestinal pathology, chronic remission and cure are achieved acute diseases stomach, intestines, liver, bile ducts, pancreas.
2. For diabetes mellitus, the glucose profile is corrected.
3. Hormonal disorders in diseases of the thyroid gland are leveled out with replacement therapy.
4. The basis of therapy for hereditary dyslipidemias is symptomatic drugs, primarily fat-soluble vitamins.
5. In case of obesity, they try to speed up the basic metabolism in the human body with the help of food, proper drinking regimen and physical activity.

In this regard, the regulation of the metabolism of fat-containing substances is carried out not by one specialist, but in a complex manner: by a therapist, a gastroenterologist, a cardiologist, an endocrinologist and, of course, a nutritionist. Together they will try to normalize lipid metabolism with folk remedies and a specific group of medications: statins, cholesterol absorption inhibitors, fibrates, bile acid sequestrants, vitamins.

 Lipid disorders

Lipids are substances of heterogeneous chemical composition. The human body contains a variety of lipids: fatty acids, phospholipids, cholesterol, triglycerides, steroids, etc. The human need for fats ranges from 80-100 g per day.

Functions of lipids

Structural: Lipids form the basis of cell membranes.

Regulatory.

† Lipids regulate membrane permeability, their colloidal state and fluidity, the activity of lipid-dependent enzymes (for example, adenylate and guanylate cyclases, Na + , K + -ATPase, Ca 2+ -ATPase, cytochrome oxidase), the activity of membrane receptors (for example, for catecholamines, acetylcholine , insulin, cytokines).

† Individual lipids - biologically active substances (for example, Pg, leukotrienes, platelet activating factor, steroid hormones) - regulate the functions of cells, organs and tissues.

Energy supply. Lipids are one of the main sources of energy for striated muscles, liver, kidneys and an additional source of energy for nervous tissue.

Protective. Included subcutaneous tissue lipids form a buffer

a layer that protects soft tissues from mechanical stress.

Insulating. Lipids create a thermally insulating layer in the surface tissues of the body and an electrically insulating sheath around nerve fibers.

Typical forms of pathology

Typical forms of lipid metabolism pathology are presented in Fig. 10–1.

Rice. 10–1. Typical forms of lipid metabolism pathology.

Depending on the level of lipid metabolism disorders, the following disorders are distinguished:

† Digestion and absorption of lipids in the gastrointestinal tract (for example, as a result of deficiency of pancreatic lipases, impaired bile formation and excretion, disorders of cavity and “membrane” digestion).

† Transmembrane transfer of lipids from the intestine to the blood and their utilization by cells (for example, with enteritis, circulatory disorders in the wall of the small intestine).

† Metabolism of lipids in tissues (for example, with a defect or deficiency of lipases, phospholipases, LPLase).

Depending on the clinical manifestations, obesity, exhaustion, dyslipoproteinemia, lipodystrophy and lipidosis are distinguished.

Obesity

The normal content of adipose tissue in men is 15–20% of body weight, in women - 20–30%.

Obesity is the excessive (pathological) accumulation of fat in the body in the form of triglycerides. At the same time, body weight increases by more than 20–30%.

According to WHO experts, in developed countries In Europe, from 20 to 60% of the population are overweight, in Russia - about 60%.

In itself, an increase in the mass of adipose tissue does not pose a danger to the body, although it reduces its adaptive capabilities. However, obesity increases the risk of ischemic heart disease (1.5 times), atherosclerosis (2 times), hypertension(3 times), diabetes (4 times), as well as some neoplasms (for example, breast, endometrial and prostate cancer).

Types of obesity

The main types of obesity are shown in Fig. 10–2.

Rice. 10–2. Types of obesity. BMI - body mass index (see text).

Depending on the degree of increase in body weight, three degrees of obesity are distinguished. In this case, the concept “ ideal mass bodies."

Various formulas are used to estimate ideal body weight.

† The simplest - index Broca : 100 is subtracted from the height indicator (in cm).

†Body mass index is also calculated using the following formula:

Body weight is considered normal with a body mass index in the range of 18.5–24.9. If these values ​​are exceeded, they are said to be overweight (Table 10–1).

Table 10–1. Obesity levels

Note. BMI - body mass index

Based on the predominant localization of adipose tissue, obesity is distinguished between general (uniform) and local (local lipohypertrophy). Types of local obesity:

† Female type (gynoid) - excess subcutaneous fat mainly in the hips and buttocks.

† Male type (android) - accumulation of fat in the abdominal area.

Based on the predominant increase in the number or size of fat cells, the following are distinguished:

† Hyperplastic obesity (due to a predominant increase in the number of adipocytes). It is more resistant to treatment and in severe cases requires surgery to remove excess fat.

† Hypertrophic (due to a predominant increase in the mass and size of adipocytes). It is more often observed after 30 years.

† Hyperplastic-hypertrophic (mixed). It is often detected in childhood.

According to genesis, primary obesity and its secondary forms are distinguished.

† Primary (hypothalamic) obesity is the result of disorders of the fat metabolism regulation system (lipostat) - an independent disease of neuroendocrine genesis.

† Secondary (symptomatic) obesity is a consequence of various disorders in the body, causing:

‡ reduction in energy consumption (and therefore the consumption of triglycerides in adipose tissue),

‡ activation of lipid synthesis - lipogenesis (observed in a number of diseases, for example, diabetes, hypothyroidism, hypercortisolism).

Causes of obesity

The cause of primary obesity is a dysfunction of the adipocyte-hypothalamus system. This is the result of a deficiency and/or insufficiency of the effects of leptin (by suppressing the production of neuropeptide Y by hypothalamic neurons, which increases appetite and hunger).

Secondary obesity develops due to excess calorie intake and P reduced level of energy consumption of the body. Energy consumption depends on the degree of activity (primarily physical) and a person’s lifestyle. Insufficient physical activity is one of the important reasons obesity.

Pathogenesis of obesity

There are neurogenic, endocrine and metabolic mechanisms of obesity.

Neurogenic variants of obesity

Neurogenic (centrogenic and hypothalamic) mechanisms of obesity are presented in Fig. 10–3.

Rice. 10–3. Neurogenic mechanisms of obesity.

† Centrogenic(cortical, psychogenic) mechanism - one of the variants of eating disorder (the other two: anorexia nervosa and bulimia). Reason: various mental disorders, manifested by a constant, sometimes irresistible desire to eat food. Possible mechanisms:

‡ activation of serotonergic, dopaminergic, opioidergic and other systems involved in the formation of feelings of pleasure and comfort;

‡ perception of food as a strong positive stimulus (doping), which further activates these systems - the vicious circle of the centrogenic mechanism of obesity development closes.

† Hypothalamic(diencephalic, subcortical) mechanism. Its cause is damage to the neurons of the ventromedial and paraventricular nuclei of the hypothalamus (for example, after a concussion, with encephalitis, craniopharyngioma, tumor metastases in the hypothalamus). The most important links in pathogenesis:

‡ Spontaneous (without an identified reason) increase in the synthesis and secretion of neuropeptide Y by neurons of the posterolateral ventral nucleus of the hypothalamus.

‡ Damage or irritation of neurons in the above-mentioned nucleus also stimulates the synthesis and secretion of neuropeptide Y and reduces sensitivity to factors that inhibit the synthesis of neuropeptide Y (mainly leptin).

§ Neuropeptide Y stimulates hunger and increases appetite.

§ Leptin suppresses the formation of the appetite stimulant - neuropeptide Y.

‡ Disruption of the participation of the hypothalamus in the formation of the feeling of hunger. This feeling is formed with a decrease in GPC, contraction of the stomach muscles during the evacuation of food and its emptying (feeling of food discomfort - “sucking in the pit of the stomach”). Information from peripheral sensory nerve endings is integrated in the nerve nuclei of the hypothalamus, responsible for eating behavior.

‡ As a result of the above processes, the production of neurotransmitters and neuropeptides that form a feeling of hunger and increase appetite (GABA, dopamine,  - endorphin, enkephalins) and/or neurotransmitters and neuropeptides that form a feeling of satiety and inhibit eating behavior (serotonin, norepinephrine, cholecystokinin, somatostatin) is enhanced ).

Endocrine variants of obesity

The endocrine mechanisms of obesity - leptin, hypothyroid, adrenal and insulin - are presented in Fig. 10–4.

Rice. 10–4. Pathogenesis of obesity.

† Leptin mechanism - leading in the development of primary obesity.

‡ Leptin formed in fat cells. It reduces appetite and increases energy expenditure by the body. The level of leptin in the blood directly correlates with the amount of white adipose tissue. Many cells have leptin receptors, including neurons of the ventromedial nucleus of the hypothalamus. Leptin suppresses the formation and release of neuropeptide Y by the hypothalamus.

‡ NeuropeptideY creates a feeling of hunger, increases appetite, reduces the body's energy consumption. There is a kind of negative feedback between the hypothalamus and adipose tissue: excess food intake, accompanied by an increase in adipose tissue mass, leads to increased secretion of leptin. This (by inhibiting the production of neuropeptide Y) reduces the feeling of hunger. However, in obese people this regulatory mechanism may be impaired, for example, due to increased leptin resistance or mutation of the leptin gene.

‡ Lipostat. The leptin-neuropeptide Y circuit ensures the maintenance of the mass of body adipose tissue - lipostat (or the body’s set point in relation to the intensity of energy metabolism). In addition to leptin, the lipostat system includes insulin, catecholamines, serotonin, cholecystokinin, and endorphins.

† Hypothyroid mechanism obesity is the result of insufficient effects of iodine-containing thyroid hormones. This reduces the intensity of lipolysis, the rate of metabolic processes in tissues and the body's energy costs.

† Adrenal(glucocorticoid, cortisol) mechanism obesity is activated due to hyperproduction of glucocorticoids in the adrenal cortex (for example, during disease or syndrome Itsenko ‑Cushing ). Under the influence of excess glucocorticoids, gluconeogenesis is activated (due to this, hyperglycemia develops), glucose transport into adipocytes, and glycolysis (lipolytic reactions are inhibited and triglycerides accumulate).

† Insulin mechanism The development of obesity develops as a result of direct activation of lipogenesis in adipose tissue by insulin.

† Other mechanisms. Obesity can also develop with other endocrinopathies (for example, with a deficiency of growth hormone and gonadotrophic hormones). The mechanisms of obesity development in these conditions are described in Chapter 27, “Endocrinopathies”).

Metabolic mechanisms of obesity

†Carbohydrate reserves in the body are relatively small. They are approximately equal to their daily intake with food. In this regard, a mechanism for saving carbohydrates has been developed.

†As the proportion of fat in the diet increases, the rate of carbohydrate oxidation decreases. This is evidenced by a corresponding decrease in the respiratory quotient (the ratio of the rate of CO 2 formation to the rate of O 2 consumption).

† If this does not happen (if the mechanism of inhibition of glycogenolysis is disrupted in conditions of a high concentration of fats in the blood), a mechanism is activated that increases appetite and increases food intake, aimed at providing the required amount of carbohydrates in the body.

†Under these conditions, fats accumulate as triglycerides. Obesity develops.

Exhaustion

Wasting and cachexia - pathological decline adipose tissue mass is below normal. At the same time, the mass of muscle and connective tissue decreases significantly.

With exhaustion, the deficit of adipose tissue can be 20–25% or more (with a body mass index below 20 kg/m2), and with cachexia - below 50%.

Causes and types of exhaustion and cachexia

There are endogenous and exogenous causes exhaustion.

Exogenous causes

† Forced or conscious complete or partial fasting (in the latter case most often for the purpose of losing weight).

‡ Complete fasting is a condition in which the body does not receive food (for example, in its absence, refusal to eat, inability to eat).

‡ Incomplete fasting is a condition characterized by a significant deficiency of plastic substances and calories in food (for example, with inadequate quantitative and qualitative nutrition, homogeneous food, vegetarianism).

† Low calorie food that does not replenish the body’s energy costs.

Endogenous causes

Depletion of endogenous origin is divided into primary and secondary.

† The causes of primary (hypothalamic, diencephalic) exhaustion are discussed in Fig. 10–5.

Rice. 10–5. The main causes of primary wasting and cachexia.

† The causes of secondary (symptomatic) exhaustion are shown in Fig. 10–6.

Rice. 10–6. The main causes of secondary wasting and cachexia.

Pathogenesis of wasting and cachexia

Exogenous wasting and cachexia. The absence or significant shortage of food products leads to the development of a chain of sequential and interdependent processes, discussed in Fig. 10–7.

Rice. 10–7. The main links in the pathogenesis of exogenous exhaustion and cachexia.

Primary endogenous forms exhaustion and cachexia. The hypothalamic, cachectic and anorexic forms are of greatest clinical importance.

† Hypothalamic form

In the hypothalamic (diencephalic, subcortical) form of exhaustion and cachexia, there is a decrease or cessation of synthesis and release of peptide Y into the blood by hypothalamic neurons. This leads to the sequential processes shown in Fig. 10–8.

Rice. 10–8. The main links of the hypothalamic mechanism of exhaustion and cachexia.

† Cachectin form

The pathogenesis of cachectin, or cytokine, form of wasting and cachexia is discussed in Fig. 10–9.

Rice. 10–9. The main links of the cachectin mechanism of exhaustion and cachexia.

† Anorexic form

The main links in the pathogenesis of the anorexic form of exhaustion and cachexia are presented in Fig. 10–10.

Rice. 10–10. The main links of the anorexic mechanism of exhaustion and cachexia.

‡ Individuals who are predisposed to developing anorexia have a critical attitude towards their body (perceived as having overweight) causes the development of neuropsychiatric disorders. This leads to prolonged episodes of food refusal. It is most often observed in teenage girls and girls under 16–18 years of age.

‡ With repeated and emotionally negative stress reactions, excessive formation of serotonin and cholecystokinin, which suppress appetite, is observed.

‡ Further course of the process can lead to the implementation of the effects of neuropeptide Y and cachectin. These factors most likely underlie the pathogenesis of anorexia nervosa. At protracted current process, a pronounced decrease in body weight develops, up to cachexia.

Secondary endogenous forms exhaustion and cachexia are important, often the main, symptoms of other pathological conditions and diseases (Fig. 10–11).

Rice. 10–11. The main causes of secondary endogenous wasting and cachexia.

Lipodystrophy

Lipodystrophy is a condition characterized by generalized or local loss of adipose tissue, less commonly by its excessive accumulation in the subcutaneous tissue. The causes of lipodystrophies are varied and not always known, from mutations of various genes (for example, lamins) to post-injection complications. There is a large group of hereditary and congenital lipodystrophy syndromes, some of them are discussed in the article “Lipodystrophies” (the “Terms Reference” appendix on the CD).

Lipidoses

Lipidoses are a typical form of lipid metabolism disorder, characterized by metabolic disorders of various lipids (for example, sphingolipidoses, gangliosidoses, mucolipidoses, adrenoleukodystrophy, leukodystrophy, lipofuscinosis, cerebrosidosis) in cells (parenchymal lipidoses), fatty tissue (obesity, emaciation) or the walls of arterial vessels (atherosclerosis). , arteriosclerosis). These forms of lipidoses are described in this textbook (Chapter 4 “Cell Damage”, in this chapter, as well as in the articles in the Appendix “Reference Book of Terms” on the CD).

Dyslipoproteinemia

Dislipoproteinemia is a condition characterized by a deviation from the norm in the content, structure and ratio of various drugs in the blood. Drug metabolism disorders are the main link in the pathogenesis of atherosclerosis, ischemic heart disease, pancreatitis and other diseases.

The nature of the course and clinical manifestations of dislipoproteinemia are determined by:

Hereditary properties of the body (for example, the composition, ratio and level of various drugs; the characteristics of their metabolism).

Environmental factors (for example, a set of food products, dietary features and eating patterns).

The presence (or absence) of concomitant diseases (for example, obesity, hypothyroidism, diabetes, kidney and liver damage).

Characteristics of lipoproteins

Various lipids circulate in the blood plasma. Free fatty acids are carried by albumin, and triglycerides, cholesterol, cholesteryl esters and phospholipids, a small amount fatty acids transported as part of the drug. These spherical particles consist of a hydrophobic core (contains cholesteryl esters and triglycerides) and a hydrophilic shell (contains cholesterol, phospholipids and apolipoproteins). The main characteristics of different drugs are given in table. 10–2.

Table 10–2. Types and main properties of lipoproteins

Apolipoproteins ensure the preservation of the ordered structure of drug micelles, the interaction of drugs with cell receptors, and the exchange of components between drugs. Detailed characteristics of apoLP and their defects are given in the article “Defects of apolipoproteins” (see the Appendix “Reference of Terms” on the CD).

Atherogenicity of lipoproteins

LPs are divided into atherogenic and antiatherogenic (Fig. 10–12).

Rice. 10–12. Types of lipoproteins depending on their atherogenicity.

The antiatherogenic effect of HDL is determined by their following properties:

† The ability to remove excess cholesterol from the plasma membrane of cells, including the vascular endothelium, and transfer it to the liver, where cholesterol is removed with bile.

† Higher affinity of HDL for apoLP E and apoLP B receptors compared to LDL. This is determined by the high content of apoLP E in HDL. As a result, HDL prevents cells from taking up cholesterol-laden particles.

Assessment of the potential atherogenicity of blood lipids is carried out by calculating the cholesterol atherogenicity coefficient:

Normally, the cholesterol atherogenic coefficient does not exceed 3.0. As this value increases, the risk of developing atherosclerosis increases.

Types of dyslipoproteinemia

The main types of dislipoproteinemia are shown in Fig. 10–13.

Rice. 10–13. Types of dislipoproteinemia.

More than 30% of primary dislipoproteinemias are inherited forms of pathology (both monogenic and polygenic with multifactorial genesis).

About 70% of dyslipoproteinemias are considered acquired. Secondary (acquired) dyslipoproteinemias are symptoms of other diseases. They accompany many human diseases (Table 10–3).

Table 10–3. The most common pathological processes leading to the development of secondary dislipoproteinemia

Various hereditary defects, as well as acquired pathological processes and diseases often lead to similar changes in the content and profile of various drugs. In this regard, fine differentiation of their origin is required, allowing for their effective treatment.

Hyperlipoproteinemia

Hyperlipoproteinemia is a condition characterized by a disorder of the formation, transport and metabolism of drugs and manifested by a persistent increase in the content of cholesterol and/or triglycerides in the blood plasma.

Classification

In 1967, Fredrickson and co-authors developed a classification of hyperlipoproteinemias (hyperlipidemias). The basis was based on data on the content of total cholesterol and triglycerides in the blood plasma, as well as the features of the distribution of drug fractions during their electrophoresis and ultracentrifugation. On this basis, five types of hyperlipoproteinemia have been identified. This classification was later revised by WHO specialists (Table 10-4).

Lipid metabolism disorders are the most common metabolic change. According to World Organization health (WHO), increased content cholesterol in the blood leads to 4.4 million deaths per year, accounting for 7.9% of total mortality.

Dyslipidemia is observed in 17-19% of the population and leads to the development of atherosclerosis, which is the cause of coronary disease hearts.

Diseases characterized by symptoms:

• hereditary dyslipidemia;
• genetic diseases accumulations: Tay-Sachs, Niemann-Pick, Gaucher disease;
• atherosclerosis in coronary heart disease;
• obesity;
• diabetes.

What are lipids and lipid metabolism

Lipids are a group of hydrophobic compounds of organic origin, including fats and fat-like substances. The lipid molecule contains fatty acids and alcohol. Lipids - component all cell membranes.

Main functions of lipids:

• energy depot;
• conduction and transmission of nerve impulses (since fats are part of the myelin sheath nerve fiber), muscle contraction;
• are predecessors organic compounds;
• protection of organs from mechanical stress;
• thermal insulation.

The main groups of lipids include:

• triglycerides;
• cholesterol;
• phospholipids;
• fatty acid.

Lipid metabolism is a complex biochemical process that occurs in several stages:

• breakdown and digestion: when fats enter with food, into small intestine Under the action of the pancreatic enzyme - lipase, fat breakdown occurs. Emulsification then occurs with the participation of bile salts;
• absorption from the intestine: some lipids are reabsorbed and enter the liver to re-form triacylglycerides, others enter the blood and lymph, binding to carrier proteins. In the blood plasma, fats are broken down into glycerol and fatty acids;
• oxidation of fatty acids: the process occurs in mitochondria with the release of ATP;
• formation of ketone bodies;
• catabolism of fatty acids.

Lipid metabolism is associated with protein and carbohydrate metabolism. The release of lipid compounds from the body occurs through the sebaceous and sweat glands.

Lipid metabolism disorders: general characteristics

A disorder of the metabolism of lipoproteins that transport fats is called dislipoproteinemia. Develops due to a violation of the ratio between different fractions of lipoproteins.

Sphingolipids, which are part of plasma membranes, are destroyed in cell lysosomes. With a genetic deficiency of enzymes that contribute to the breakdown of sphingolipids, accumulation of incomplete breakdown products occurs in lysosomes. Such storage diseases include Tay-Sachs, Gaucher, and Niemann-Pick diseases.

Atherosclerosis - pathological process, which is accompanied by the formation of atherogenic plaques on the inner lining of blood vessels. It develops as a result of a violation of the intake and excretion of cholesterol, and is also associated with a violation of the ratio of high and low density lipoproteins. Because LDL (low-density lipoprotein) transports cholesterol into tissues, and HDL (high-density lipoprotein) transports cholesterol out of tissue. Therefore, in dyslipidemia, LDL levels are increased and HDL levels are decreased.

Etiology

Lipid metabolism disorders occur due to several reasons:

• deficiency of enzymes involved in the synthesis or breakdown of fats;
• reduction in the amount of transport proteins;
• increased synthesis individual species lipids;
• hormonal disorders leading to impaired fat metabolism;
• increased intake of lipids into the body from food.

Most often, there is a complex pathology leading to a failure of lipid metabolism.

Classification

Lipid metabolism disorders can be primary or secondary. Primary is diagnosed in people on early stage formation of atherosclerosis, secondary - develops with excessive consumption of cholesterol from food, a passive lifestyle, or the presence of a hereditary predisposition.

Kinds improper metabolism fat:

• isolated hypercholesterolemia;
• mixed hyperlipidemia;
• isolated hypertriglyceridemia.

Diagnostics

An examination is carried out, the patient is interviewed about organs and systems, measurements blood pressure. An anamnesis is collected to identify risk factors, and the body mass index is calculated. To diagnose the conditions that cause dyslipidemia, additional studies will be needed:

• clinical analysis of blood, urine;
• serum glucose;
• biochemical analysis blood: total cholesterol, triglycerides, low and high and very low density lipoproteins and atherogenicity coefficient;
• thyroid hormones;
• genetic tests to determine gene mutations.

Often, an in-depth examination reveals metabolic syndrome. It includes increased blood pressure, obesity, impaired glucose tolerance and dyslipidemia.

Treatment

Lipid metabolism disorders are treated comprehensively:

• normalization of body weight;
• rationalization of nutrition;
• refusal bad habits;
• sufficient motor mode;
• taking lipid-lowering drugs.

To achieve target lipid profile levels, the following drugs are used:

• statins (Atorvastatin, Simvastatin, Rosuvastatin, Lovastatin) have been proven to be effective and influence the regression of atherosclerotic vascular lesions;
• a nicotinic acid;
• fibrates (Bezafibrate, Ciprofibrate and Fenofibrate);
• bile acid sequestrants (Colestyramine, Colestipol, Colesevelam);
• antioxidants (vitamin A, E, C).

Rational nutrition and weight loss come first for this pathology.

Diet

To reduce body weight and cholesterol levels, you must adhere to the following recommendations:

• nutrition in small portions 4-5 times a day;
• sufficient drinking regime 1.2-2 liters of liquid per day, drink a glass of water in the morning on an empty stomach;
• exclude products made from wheat flour, baked goods, milk and fatty dairy products. You should not eat sausages fatty types meat (pork, lamb). It is not recommended to fry foods in animal fats, use ready-made sauces, mayonnaise, smoked products;
• It is recommended to consume bread and pasta made from whole grain flour. Introduce fish, vegetables and fruits, soups, cereals, meat (rabbit, chicken, turkey) into your diet. Use dairy products with 1-4% fat content.

Physical education and massage

In the complex therapy of dyslipidemia, physical therapy is indicated, which solves the following problems:

• slows down the progression of the disease;
• improves blood flow and adapts cardiovascular system to loads;
• body weight decreases.

Well physical therapy appointed for a certain period. After completion, the patient maintains adequate physical activity: walking at an average pace of 2-3 km with ups and downs is recommended.

Massage is prescribed twice a year in courses of 10-15 sessions, lasting 20-30 minutes. The maximum effect is observed when performing physical therapy exercises and massage.

Treatment with folk remedies

In the treatment of lipid metabolism failure, infusions and decoctions are used:

• pour a teaspoon of lemon balm, mint, nettle and strawberry leaves into 400 ml of boiling water and leave for an hour. Take a glass a day, divided into 3 doses;
• Pour 30 g of fireweed tea into 0.5 liters of boiling water and leave for 30 minutes. Take 70 ml 4 times a day;
• Art. Pour 300 ml of boiling water over a spoonful of burdock leaves and leave for an hour. Take throughout the day.

Doctor's advice. Folk remedies are not used as monotherapy. If you experience symptoms of changes in fat metabolism, you should consult a doctor.

Consequences and complications

Dyslipidemia is often asymptomatic or patients do not seek help in a timely manner. The most common complications of this pathology:

• atherosclerosis of the heart vessels, which leads to myocardial infarction;
• damage to the blood vessels of the brain, resulting in hemorrhage or ischemic stroke;
• blood clot formation.

Important! Disorders of lipid metabolism are rare independent disease. More often, pathology signals the presence of an underlying disease. The main symptoms are obesity, fatty nodules on the face and enlarged liver. To diagnose the underlying disease, you need to see a therapist and undergo additional examinations. Therapy for metabolic failure of fat-containing compounds consists of following healthy image life and taking lipid-lowering drugs.

Prognosis and prevention

• weight loss;
• a diet with reduced cholesterol content of animal origin;
• physical activity;
• taking lipid-lowering drugs.

If you adhere to the basic rules and undergo a doctor's examination on time, the risk of complications will be minimized.

Lipid metabolism is the process by which fatty acids are metabolized, broken down to generate energy or stored in the body as a source of energy for future use. Fatty acids are components of triglycerides, which make up most of the fats consumed by humans in foods such as vegetable oils and animal products. Triglycerides are found in blood vessels or stored for future use as an energy source in adipose tissue cells, more commonly known as body fat, and also in liver cells.

Although carbohydrates are the main source of energy, when their reserves are depleted, fatty acids in triglycerides begin to be broken down and used as a reserve source of energy. For example, the body draws energy from fats when performing physical exercise, when glycogen stores (or the form of carbohydrate-derived glucose that is suitable for storage) are running low, or when the amount of carbohydrates in the diet is insufficient to meet the body's energy needs.

Remember, fat is not eliminated from the body by itself...

Triglycerides, also known as lipids or fats, are a good source of energy because each gram contains 9 calories (37 kilojoules), while one gram of carbohydrates contains only 4 calories (17 kilojoules).

Since calories are units of energy, fats are considered energy-dense nutrients. Triglycerides are made up of three chains of fatty acids linked to a hydrogen-containing compound called glycerol. When the body requires additional calories, these fatty acids are released through fat metabolism.

Where does fat metabolism begin in the body...

The first stage of fat metabolism is the consumption and absorption of triglycerides, which are also found in foods plant origin, such as olives, nuts and avocados, and in animal products such as meat, eggs and dairy products.

These fats reach digestive tract into the intestine, but they cannot be absorbed there in the form of triglycerides. Therefore, they are broken down by an enzyme called lipase into fatty acids, most often monoglycerides, which are one chain of fatty acids connected to glycerol. The broken down triglycerides are then absorbed into the body through the intestines and return to their original form before being transported to the lymphatic system by chylomicrons, a type of substance similar to cholesterol known as lipoproteins.

From lymphatic system triglycerides enter the bloodstream, where the process of fat metabolism can be completed in one of three ways - triglycerides are either transported to the liver, or to muscle cells, or to fat cells, where they are either stored or used as a source of energy. If they enter liver cells, they are converted into “bad” cholesterol, known as very low-density lipoprotein, and released into the bloodstream, where they transport other lipids. Triglycerides that end up in muscle cells can be oxidized in the mitochondria of those cells and used for energy, while those that end up in fat cells are stored until needed later. This leads to an increase in the size of fat cells, which manifests itself as large quantity body fat.